What is surfer’s myelopathy, its clinical presentation, and the recommended acute management?

Surfer's Myelopathy (Acute Hyperextension-Induced Myelopathy)

Surfer's myelopathy is a rare, non-traumatic spinal cord ischemia that causes acute paraparesis or paraplegia in novice surfers, with only a 42% complete neurological recovery rate, making early recognition critical to prevent permanent disability 1.

What It Is

Surfer's myelopathy, now also termed acute hyperextension-induced myelopathy (AHIM), is a vascular spinal cord injury affecting the lower thoracic cord and conus medullaris (typically T8-T12) 2, 3. Despite its name, this condition can occur with any activity involving sustained or repeated spinal hyperextension—including yoga, Pilates, gymnastics, and ballet 2.

Pathophysiology

The mechanism involves vascular insufficiency from dynamic compression of the artery of Adamkiewicz during hyperextension 2. In surfing specifically, the combination of:

• Prolonged prone positioning with back hyperextension (the "pop-up" maneuver)
• Valsalva maneuver execution while standing on the board
• Increased intraspinal pressure

...leads to arterial compression and/or in situ thrombosis 4. Recent evidence suggests venous congestion may also contribute, as demonstrated by ADC hyperintensity without diffusion restriction on MRI 5.

Clinical Presentation

Classic Triad

1. Acute lower back pain during or immediately after the hyperextension activity
2. Rapid progression to paraparesis/paraplegia (within minutes to hours)
3. Urinary retention and bowel dysfunction

Key Clinical Features

• Demographics: Young, healthy individuals (average age 25 years) with no pre-existing spinal disease 3
• Timing: Almost exclusively first-time participants in the activity 1, 3
• Sensory findings: Bilateral hypesthesia/hypalgesia or hyperesthesia below the groin, typically with a sensory level at T10 4
• Motor findings: Ranges from incomplete paraparesis to complete paraplegia (>50% present with complete deficits) 1
• Severity at presentation dictates prognosis—ASIA A patients show no improvement, while incomplete cases may improve within 24 hours 1

Critical Pitfall

The non-traumatic nature makes diagnosis easily missed. Patients may not connect their neurological symptoms to the preceding activity, especially if symptom onset is delayed by several hours 2.

Diagnostic Evaluation

Immediate Imaging: MRI Spine

Order MRI of the entire spine (cervical, thoracic, lumbar) without and with IV contrast immediately 6. This is the gold standard and "usually appropriate" initial imaging for acute myelopathy 6.

MRI Timing and Findings

• T2-weighted images: Central cord hyperintensity from T8 to conus medullaris appears within 6-24 hours, peaks at day 3, then gradually resolves 7
• Diffusion-weighted imaging (DWI): Include this sequence—it can show signal changes earlier than T2 images and helps differentiate arterial vs. venous ischemia 6, 5
• ADC mapping: Hyperintensity without diffusion restriction suggests reversible venous ischemia and may indicate better prognosis 5
• Gadolinium enhancement: Not helpful in early acute phase; absence of enhancement doesn't rule out ischemia 1

Important: Lesion expansion on serial MRI in the first 3 days is expected and does not necessarily indicate treatment failure 7.

Additional Vascular Imaging

Consider CT angiography or MR angiography of the thoracic/lumbar spine to document vascular occlusions or stenosis of segmental arteries 6, 4. While underutilized historically 1, angiography can confirm the vascular etiology by demonstrating:

• Absence or occlusion of radicular arteries (T11-L2 levels)
• Absent artery of Adamkiewicz
• Segmental artery stenosis

Differential Diagnosis to Exclude

The imaging and clinical workup must rule out:

• Spinal cord compression (disc herniation, epidural hematoma/abscess)
• Demyelinating disease (MS, NMO, ADEM)
• Infectious/inflammatory myelitis
• Fibrocartilaginous embolism
• Spinal AVM rupture

Acute Management

Hemodynamic Support

Maintain mean arterial pressure (MAP) ≥70 mmHg continuously for the first 5-7 days 8. This recommendation comes from French guidelines for spinal cord injury management, which showed correlation between MAP >70 mmHg and improved neurological outcomes 8.

• Use continuous arterial line monitoring
• Avoid any episodes of systolic BP <110 mmHg, as hypotension is an independent mortality predictor 8
• Target spinal perfusion pressure >50 mmHg if intrathecal pressure monitoring available

Pharmacological Interventions

Administer high-dose intravenous methylprednisolone despite limited evidence specific to surfer's myelopathy 1, 7, 4. The systematic review found that 55% of patients receiving steroids improved with no reported adverse effects 1. Typical regimen:

• Methylprednisolone 30 mg/kg IV bolus
• Followed by 5.4 mg/kg/hour infusion for 23-48 hours

Consider antiplatelet therapy and/or anticoagulation given the vascular etiology 5, 4. While not universally studied, case reports document use of:

• Aspirin 81-325 mg daily
• Therapeutic anticoagulation in select cases with documented thrombosis

Adjunctive neuroprotective agents used in case reports include:

• IV glycerol for edema reduction 7
• IV edaravone (free radical scavenger) 7

Supportive Care

• Bladder management: Intermittent catheterization for urinary retention
• Bowel regimen: Aggressive bowel program to prevent constipation
• DVT prophylaxis: Pharmacologic and mechanical prophylaxis
• Pressure injury prevention: Turn every 2 hours, specialized mattress

Transfer to Specialized Center

Transfer immediately to a Level 1 trauma center or specialized spinal cord injury unit 8. Direct admission to specialized centers reduces morbidity, mortality, and improves neurological outcomes for spinal cord injuries 8.

Prognosis and Recovery Timeline

Prognostic Factors

The severity at presentation/nadir is the single most important prognostic factor 1:

• ASIA A (complete) at presentation: No reported improvement in any case series
• Incomplete deficits: 42% overall complete recovery rate; many improve within 24 hours 1, 3
• Near-complete recovery: Typically occurs in 3-4 patients out of 9 in case series 3
• Residual deficits: Common findings include mild weakness, persistent urinary retention, and sensory changes

Recovery Timeline

• Motor function improvement: Begins at 3 weeks, continues through 8+ weeks 7, 9
• MRI resolution: Complete signal normalization by 8 weeks 4
• Important lag: Imaging improvement precedes clinical improvement 7

Rehabilitation

Initiate comprehensive inpatient rehabilitation immediately after acute stabilization (within 10 days) 9. A structured 10-day intensive program in a pediatric case showed exceptional functional mobility improvement 9.

Prevention and Awareness

The most effective intervention may be prevention through education 1. Risk factors to communicate to novice participants:

• First-time surfing, yoga, gymnastics, ballet
• Prolonged prone positioning with back hyperextension
• Repetitive "pop-up" movements
• Inadequate warm-up or conditioning

Instructors should be educated to recognize early warning signs (acute back pain during activity) and immediately cease the activity.